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Biomedical subjects

A E Tattersfield

Publications and source records attributed to A E Tattersfield.

At least 19 recordsLinked to original sources
PubMed1995

Dietary antioxidant vitamin intake and lung function in the general population.

We have investigated the relation between lung function and dietary intake of the antioxidant vitamins C and E in the general population in a cross-sectional survey of a random sample of adults from the electoral register of an administrative area of Nottingham. In 2,633 subjects 18 to 70 yr of age, we measured FEV1 and FVC, allergen skin sensitivity to grass pollen, cat fur, and Dermatophagoides pteronyssinus, pack-years smoking exposure by personal recall, and usual dietary intake of vitamins C and E by semiquantitative food frequency questionnaire. After adjustment for the effects of age, sex, height, mean allergen skin wheal diameter, and pack-years smoking history, both FEV1 and FVC were significantly and independently related to mean daily intake of vitamin C, such that a standard deviation (40 mg/d) higher vitamin C intake was associated with a 25.0 (95% CI, 5.2 to 44.8; p = 0.01) ml higher FEV1 and a 23.3 (0.94 to 45.7, p = 0.04) ml higher FVC. There was also an association between vitamin E intake and lung function, such that a standard deviation (2.2 mg) higher intake of vitamin E was associated with a 20.1 (1.3 to 40.4, p = 0.04) ml higher FEV1 and a 23.1 (1.0 to 45, p = 0.04) ml higher FVC. However, vitamin C and vitamin E intakes were significantly correlated (r = 0.29, p < 0.001), and after allowing for the effects of vitamin C there was no additional independent effect of vitamin E on either FEV1 or FVC.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1994

Safety and efficacy of nebulized lignocaine in patients with cancer and breathlessness.

Although anecdotal reports suggest nebulized lignocaine may help breathlessness in patients with cancer this has not been examined formally. We report a pilot study comparing nebulized lignocaine 100 mg and 200 mg with saline in six patients with cancer who were breathless at rest. Nebulized lignocaine was well tolerated apart from mild bronchoconstriction in two patients after the 200 mg dose and the unpleasant taste; serum concentrations were below levels at which toxicity has been reported. The effort of breathing (measured on a visual analogue scale) did not differ between treatments, whereas the distress of breathing was less after saline than after either dose of lignocaine. These findings do not support the reported benefits of nebulized lignocaine.

Administration, Intranasal↗
PubMed1992

Effect of oral lithium on bronchial reactivity in asthma.

1. Recognition that inositol phospholipid-derived second messengers are involved in the initiation and maintenance of airway smooth muscle contraction raises the possibility of new therapeutic approaches to the treatment of asthma. We anticipated that lithium, through its effects on cell signal transduction and ion-transport pathways, would be likely to protect the airways against constrictor stimuli. 2. We carried out a randomized, double-blind study of lithium carbonate in asthmatic patients. 3. After a 1 week run-in period, 27 patients were allocated lithium carbonate (800 mg) or placebo for 21 days with measurement of forced expiratory volume in 1 s, the dose of histamine causing a 20% fall in the forced expiratory volume in 1 s and serum lithium concentration on days 3, 7, 14 and 21. 4. Twenty-one patients completed the study (10 on lithium, 11 on placebo). Mean serum lithium levels for patients on active treatment were in the therapeutic range on all four occasions. 5. Lithium did not alter the forced expiratory volume in 1 s (P = 0.8) or the twice-daily peak expiratory flow (P = 0.15). It did, however, reduce histamine reactivity (the maximum difference between lithium and placebo was 1.2 doubling doses of histamine on day 21; 95% confidence interval 0.2-2.2 doubling doses), improve symptom scores (P less than 0.05) and reduce usage of beta-adrenoceptor agonist inhalers (P less than 0.05). 6. We conclude that lithium reduces bronchial reactivity in airway smooth muscle; this finding raises new therapeutic possibilities for the treatment of asthma.

Administration, Oral↗
PubMed1992

Asthma. Bronchodilators: new developments.

This chapter is concerned with recent controversies and new developments in the area of established bronchodilators, namely beta-agonists, antimuscarinic drugs and methylxanthines. It focuses on the studies concerned with fenoterol and its possible role in asthma deaths in New Zealand, the new long-acting beta-agonists and the place of beta-agonists in the treatment of asthma. The possible reasons for the fact that antimuscarinic drugs have been less effective in general than beta-agonists in asthma are explored and the difficulties of using theophylline in clinical practice and its role in the treatment of asthma are discussed.

Adrenergic beta-Agonists↗
PubMed1992

Inhaled frusemide and exercise induced asthma: evidence of a role for inhibitory prostanoids.

BACKGROUND: Inhaled frusemide protects subjects with asthma against a wide range of bronchoconstrictor challenges, including allergen, exercise and inhaled sodium metabisulphite. An investigation was designed to determine whether this protection is related to the production of inhibitory prostaglandins, such as prostaglandin E2 (PGE2), by studying the effect of the cyclooxygenase inhibitor indomethacin on the protection afforded by inhaled frusemide against exercise induced asthma. METHODS: In a double blind crossover study 10 subjects with mild asthma were pretreated with indomethacin (50 mg thrice daily) or placebo capsules for three days; they then inhaled frusemide (40 mg) or placebo 10 minutes before an exercise test previously shown to cause a 20-30% fall in forced expiratory volume in one second (FEV1). RESULTS: After inhalation of placebo exercise caused a similar maximum fall in FEV1 whether pretreatment was with placebo (26%) or indomethacin (25.2%). After inhalation of frusemide the maximum fall in FEV1 was reduced to 14.3% after placebo pretreatment and to 21.8% after indomethacin pretreatment; the difference between placebo and indomethacin pretreatment was significant (mean difference 7.5%, 95% limits 0.6%, 14.4%). The inhibitory effect of frusemide on the response to exercise, assessed as change in FEV1 over 30 minutes, was significantly greater with placebo (62%) than indomethacin (13%) pretreatment. CONCLUSION: These findings support a role for inhibitory prostanoids, such as PGE2, in the beneficial effects of frusemide as a protection against exercise induced asthma.

Administration, Inhalation↗
PubMed1992

Modification of bronchial reactivity by physiological concentrations of plasma epinephrine.

Circulating epinephrine concentrations are altered in certain pathophysiological states, but whether such changes in epinephrine concentrations can alter bronchial responsiveness in subjects with asthma has not been studied. We studied 10 subjects with asthma in a double-blind crossover study on 4 nonconsecutive days. After measurement of baseline forced expiratory volume in 1 s (FEV1) and plasma epinephrine concentration, subjects were given placebo or 4, 16, or 64 ng.kg-1.min-1 epinephrine by intravenous infusion for 45 min. Blood was taken for plasma epinephrine concentration before the infusion and at 30 min, when a histamine challenge test was performed. Mean plasma epinephrine concentrations ranged from 0.37 nmol/l on placebo to 3.76 nmol/l with the 64-ng/kg infusion. FEV1 increased progressively with increasing concentrations of infused epinephrine, the mean change ranging from -0.051 on placebo to 0.331 after the highest concentration of epinephrine. The provocative dose of histamine causing a 20% fall in FEV1 increased progressively with increasing concentrations of infused epinephrine, geometric mean values ranging from 0.61 mumol with placebo to 1.7 mumol after the highest dose of epinephrine. Thus epinephrine, at physiological plasma concentrations, can modify bronchial reactivity.

Adult↗
PubMed1992

Comparison of bronchial reactivity and peak expiratory flow variability measurements for epidemiologic studies.

Inclusion of a standardized measurement of airway function is important in epidemiologic studies of asthma to facilitate comparison between different studies. Bronchial reactivity is widely used in such studies, but measurement of peak expiratory flow (PEF) variability has a number of potential advantages. We compared PEF variability with methacholine challenge tests in a community population sample. Subjects selected at random (n = 95) and on the basis of having experienced wheeze in the last 12 months (n = 130) performed a challenge test with methacholine to a maximum dose of 12.25 mumol and made serial PEF recordings every 2 h for a week. PEF variability was expressed as mean daily maximum amplitude as a percentage of the mean (amplitude % mean). Increased bronchial reactivity and PEF variability were arbitrarily defined as values above the 10th or below the 90th percentiles in the random sample. A measurement of amplitude % mean was available from all 225 subjects, whereas only 115 (51%) had a measurable PD20 methacholine. PD20 measurements correlated weakly but significantly with amplitude % mean (r = -0.44, p less than 0.001). Increased values of both bronchial reactivity and PEF variability were related to the presence of respiratory symptoms in the week before testing. Asthma was more strongly related to increased bronchial reactivity than to PEF variability. Both measurements showed a strong association with atopy and the intraclass correlation coefficients (ratio of between-subject to total variance) were similar for both.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1991

Respiratory function in the elderly and the effects of beta blockade.

Bronchoconstriction, the main respiratory side effect from beta-blocking drugs, can be severe and precipitous in patients with asthma, but at most is very minor in patients with chronic bronchitis. Elderly patients with asthma and chronic bronchitis appear to run a similar risk from beta-blocking drugs as younger patients with these conditions, though there are no direct comparisons. Several studies have looked at the response of elderly patients to beta-blocking drugs, and the profile and incidence of respiratory side effects has been similar to those seen in studies of younger subjects. There is a greater danger in the elderly that a past history of asthma may be overlooked or that bronchoconstriction from a beta-blocking drug is attributed to other causes.

Adrenergic beta-Antagonists↗
PubMed1991

Effect of RG 12525, an oral leukotriene D4 antagonist, on the airway response to inhaled leukotriene D4 in subjects with mild asthma.

We have studied the effect of RG 12525, an oral leukotriene D4 (LTD4) antagonist, on LTD4-induced bronchoconstriction in eight male subjects with mild asthma (baseline FEV1 greater than 80% predicted) in a double-blind, placebo-controlled fashion. RG 12525 800 mg displaced the dose-response curve for LTD4 to the right. The mean (95% confidence intervals) difference in log PC20FEV1 following RG 12525 and placebo was 2.88 (1.61, 4.17) doubling doses of LTD4 (P less than 0.01), a 7.5 fold difference. We conclude that RG 12525 when administered orally is an effective LTD4 antagonist in subjects with mild asthma.

Administration, Oral↗
PubMed1991

Effect of inhaled budesonide on bronchial reactivity to histamine, exercise, and eucapnic dry air hyperventilation in patients with asthma.

BACKGROUND: It has been suggested that inhaled corticosteroids may provide greater protection against constrictor stimuli that act indirectly such as exercise than those that act directly such as histamine. METHODS: The effects of six weeks treatment with inhaled budesonide (800 micrograms twice daily) on bronchial reactivity to histamine, exercise, and eucapnic voluntary hyperventilation of dry air were compared in a double blind, placebo controlled, non-crossover study in 40 subjects with asthma. Change in bronchial reactivity to histamine and eucapnic hyperventilation over the six weeks was measured as change in the provocative dose of histamine or dry air causing a 20% fall in FEV1 (PD20 histamine and PV20 eucapnic hyperventilation (EVH) of dry air); this was not possible for exercise because of the development of refractoriness. To enable the change in response to all three stimuli to be compared, the response (percent fall in FEV1) to a fixed dose was measured for all three challenge tests. RESULTS: After budesonide there was an increase in PD20 histamine from 0.48 to 2.81 mumol and in PV20 EVH from 364 to 639 litres, and a significant correlation between the changes in PD20 histamine and PV20 EVH (r = 0.63). The median percentage fall in FEV1 in response to eucapnic hyperventilation, exercise, and histamine was similar before budesonide (25.5%, 26.6%, and 24.5%); the reduction in the percentage fall in FEV1 with budesonide was also similar for the three challenges (18.9%, 17.5%, and 16.6%), and all differed significantly from the changes following placebo. There was a significant correlation between change in percentage fall in FEV1 after budesonide with the three stimuli (histamine v exercise: r = 0.48; histamine v eucapnic hyperventilation: r = 0.46; exercise v eucapnic hyperventilation: r = 0.63). CONCLUSION: The similar magnitude of change in bronchial reactivity to all three stimuli after budesonide and the within subject correlation obtained between these changes suggest that corticosteroids act by a common mechanism to protect against eucapnic hyperventilation, exercise, and histamine.

Administration, Inhalation↗
PubMed1991

Effect of inhaled prostaglandin E2 on bronchial reactivity to sodium metabisulphite and methacholine in patients with asthma.

Inhaled frusemide protects against the bronchoconstrictor response to a wide range of stimuli that cause bronchoconstriction by indirect mechanisms. One possible explanation for this protection relates to the known ability of frusemide to enhance synthesis of prostaglandin E2 (PGE2). Studies in vitro suggest that PGE2 might protect against indirectly acting bronchoconstrictor challenges rather than those that act directly on airway smooth muscle, though little is known about the effects of PGE2 in vivo. The effect of inhaled PGE2 on the bronchoconstrictor response to inhaled sodium metabisulphite (a stimulus with an indirect action) and methacholine (which acts directly on airway smooth muscle) was studied in nine patients with asthma. Subjects were studied on four days, inhaling PGE2 (100 micrograms) or placebo in a double blind fashion followed immediately by a cumulative dose challenge with sodium metabisulphite or methacholine. The response to the constrictor stimuli was measured as the provocative dose causing a 20% fall in FEV1 (PD20). There was no significant change in FEV1 after inhaled PGE2 compared with placebo, nor any significant change in the response to methacholine; the geometric mean methacholine PD20 was 0.9 mumol after PGE2 and 0.56 mumol after placebo (mean difference 0.7 (95% confidence limits--0.1, 1.5) doubling doses). PGE2, however, protected against sodium metabisulphite, the geometric mean sodium metabisulphite PD20 being 11.8 mumol after PGE2 and 1.8 mumol after placebo (mean difference 2.5 (95% CL 1.9, 3.1) doubling doses). PGE2 conferred significantly greater protection against sodium metabisulphite than methacholine (mean difference 1.8 (95% CL 0.8, 2.8) doubling doses). This suggests that PGE2, like frusemide, has an inhibitory effect on pathways relevant to the bronchoconstriction induced by sodium metabisulphite, with little or no effect on those relevant to methacholine.

Adolescent↗